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Cardio - Gupta > Pathology of Hypertension > Flashcards

Pathology of Hypertension Flashcards

1
Q

Hyaline Ateriolosclerosis

  • Associated with what disease?
  • Cause?
  • Patient Profile?
  • Appearance?
A

Disease Association:

• Benign Hypertension

Cause:

  • Pressure pushes plasma proteins across injured endothelial cells
  • Chronic Stress ^ increases matrix synthesis

Patient Profile:

• Hypertensive patients or Old people

Appearance:

• Thick Intima with very pink appearance from deposited proteins

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2
Q

Hyperplastic Arteriolosclerosis

  • Associated with what disease?
  • Cause?
  • Appearance?
A

Disease Association:

• SEVERE (malignant) Hypertension

Cause:

  • Increased strain causes Muscle cells to become thickened and duplicated
  • FIBRINOID NECROSIS may also occur

Appearance:

  • Onion Skinning appearance
  • Amphoric and pink in the case of fibrinoid necrosis
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3
Q

Thrombosis

• cause of thrombosis in Vascular Disease?

A

Formation of a Blood Clot from Exposed ECM

• in this context Exposed ECM comes from ruptured plaque

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4
Q

Embolus

• cause?

A

Thrombus is mobilized and can move throughout vasculature

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5
Q

Atherolsclerosis

A
  • Disease characterized by Intimal Lesions called artheromas
  • these artheromas have a lipid core surrounded by a fibrous cap
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6
Q

Medial Calcific Sclerosis

A
  • Common in people over 50 y/o where Calcium is seen in the intima
  • Don’t freak out if you see this on a radiograph or mammogram as long as it follows a vessel its okay
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7
Q

What is the significance of: Turbulence, Dyslipidemia

A

• Two most common causes of endothelial injury leading to atherosclerosis

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8
Q

What is a Fatty Streak?

A

i

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9
Q

What is a Plaque?

A

i

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10
Q

What is Stenosis?

A

Occlusion of an artery caused by large atherosclerotic plaque

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11
Q

Aneurysm

A

Ballooning out of all 3 layers of a vessel due to weakening of the media

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12
Q

Dissection

A

i

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13
Q

T or F: Hypertension puts you at an increased risk for renal failure?

A

True, this risk is especially high in people with diabetes and hypertension

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14
Q

What are the cutoffs for hypertension?

A

140 mmHg systolic 90 mmHg diastolic

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15
Q

In what case might you place a patient with a blood pressure of lower than 140/90 on anti-hypertensive medication?

A

• High risk patients such as those with Diabetes may need treatment earlier than other people

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16
Q

T or F: in the case of hypertension preventative medicine has proven to be extremely effective.

A

True

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17
Q

What causes most cases of hypertension?

A

90% of cases are idopathic

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18
Q

What are some diseases that often have a secondary effect of hypertension?

A

• Renal Disease

• Renal Artery Narrowing

• Adrenal Disorders

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19
Q

Why is hypertension often a secondary result of many renal disorders?

A
  • Macula Densa falsely Sense Low Blood Volume because of renal disease
  • Increased Renin –> angiotensin I –> angiotensin II will lead to increased fluid volume and a heart that is beating harder
  • Aldosterone may be secreted in too large amount in adrenal tumors etc. (pheochromocytoma)
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20
Q

How do you calculate Cardiac Output?

A

CO = Heart Rate x Stroke Volume

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21
Q

What is the standard response of the vascular wall to injury?

A
  • Smooth Muscle Hyperplasia in INTIMA
  • ECM is synthesized
  • PERMANENT intimal thickening result
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22
Q

Atherosclerosis

  • Cause
  • Vessels involved
  • Disease Type
A

Cause:

• LIPID Accumulation with Cellular Reaction

Vessels Involved:

• Large and Medium Arteries

Disease Type:

• Considered an INFLAMMATORY DISEASE

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23
Q

What are the most common arteries to see atherosclerosis in?

A

• Abdominal Aorta

• Coronary Arteries

• Cerebral

• Common Iliac

• Femoral Arteries

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24
Q

****What is this?

• Clinical Significance

A

Monckebergs

• Typically not clinically significant

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25
Q

**Monckebergs

  • Cause
  • Vessel type
  • Appearance (radiology and H&E)
  • Significance
A

Cause:

• Cacification of Vessel Media

Vessel:

• Muscular Arteries

Appearance:

  • Dark purple calcium deposits in the media on H and E
  • Follows the path of the vessel on Radiology
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26
Q

What patient population is Monckenbergs often seen in ?

A

• Ppl. 50 years and older commonly have Monckebergs

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27
Q

**Arteriolosclerosis

  • Cause
  • Vessel type
  • Types
A

Cause:

• Reduced lumen size from thickening of vessel in response to high pressure

Vessel Type:

• Small Arteries

2 types:

• Hyaline

• Hyperplastic

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28
Q

What diseases are associated with arteriolosclerosis?

A
  • Diabetes
  • Hypertension
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29
Q

****What is this?

• key features?

A

Nephrosclerosis

• Pitting Scars on the surface that should be smooth

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30
Q

****What is this?

• Patients this is most commonly seen in?

A

Onion Skinning in Hyperplastic Arteriolosclerosis

• Most commonly seen in patients with malignant hypertension (>200mmHg systolic)

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31
Q

*****What is this?

• Patients this is most commonly seen in?

A

Hylaine arteriolosclerosis - intimal thickening from ECM expansion

• seen in Elderly and people with Benign Hypertension

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32
Q

*****What is this?

• Patients this is most commonly seen in?

A

Hyperplastic arteriolosclerosis that has caused Fibrinoid Necrosis of Small Renal Arteries

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33
Q

What organs are most commonly damaged in Hyperplastic Arteriolosclerosis?

A

Kidney Damage is common

34
Q

What is an atheroma?

A

• Plaques of LIPID CORES covered by a FIBROUS CAP • Lesions found in the INTIMA

35
Q

What is the difference in etiology of an acute occlusion vs. chronic occlusion of a large vessel lumen?

A

Chronic:

• Plaque slowly builds up by binding more and more LDL

Acute:

• Cap ruptures and underlying collagen etc. is exposed and leads to acute Myocardial Infarction

36
Q

How can atheroclerotic plaques increase the probability of aneurysm?

A

• Lipids and Necrotic Tissue may weaken the intima and media causing a ballooning out (aneurysm) of the vessel

37
Q

What are some of the constitutional risk factors for atherosclerosis?

A

Genetics:

  • Mendelian Disorders (like FH)
  • Polygenic traits (like Diabetes, HTN)

Age:

• 40-60 pts. may start to become symptomatic Gender: • Premenopausal Women are protected

38
Q

What are some modifiable risk factors for atherosclerosis?

A
  • Hyperlipidemia
  • Hypertension
  • Cigarettes
  • Diabetes
  • Inflammation (CRP and Hyperhomocysteinemia)
39
Q

What is the first gross sign indicating where a clot might form?

A

• Fatty Streak

40
Q

**What are the steps in formation an atherlosclerotic plaque?

A
  • Chronic Endothelial Injury
  • Endothelial Dysfunction attracts leukocytes, monocytes, and platelets
  • Macrophages Recruit Smooth Muscle to the intima
  • Macrophages and Smooth Muscle Cells eat LIPIDS
  • Smooth muscle cells proliferate and deposit Collagen and ECM
41
Q

What is secreted by T-cell in the atherlosclerotic plaque?

A

IFN-gamma

42
Q

What does the fibrous plaque resemble underneath the microscope?

A

Granulation Tissue

43
Q

What is the difference in stable and and unstable progression of atherloma?

A

Stable:

• Slow progression caused by accumulation of more and more lipid in the intima

***Leads to stable angina

Unstable:

• RAPID progression caused by platelet and fibrin deposition that expands and causes thrombus formation

44
Q

How do you know a plaque is becoming unstable?

A

• 70% or more of the lumen is occluded - this characterizes and unstable plaque

45
Q

What vessels are most commonly involved in Atherlosclerosis?

A
  • INFRARENAL abdominal Aorta
  • Coronary Arteries
  • Popliteal Arteries
  • Internal Carotid Arteries
  • Circle of Willis
46
Q

What are the ways in which Athlerosclerosis become clinically relevent?

• when does this happen?

A

40-60 y/o Disease Becomes Clinically Relevent 3 ways:

  • Aneurysm (weakening of arterial wall)
  • Thrombosis (ruptured plaque)
  • Critical Stenosis (>70% vessel occlusion)
47
Q

****What is this?

A

• Atherosclerotic Plaque

48
Q

What are the 3 most common areas where plaques occur?

A

• Ostia of Existing Vessels
• Branch Points
• Posterior Wall of Abdominal Aorta

49
Q

What roles does dyslipidemia play in formation of atherosclerotic plaque?

A
  • Cholesterol impairs endothelial cell function causing an increase in free radicals that scavenge NO leading to less vasodilation
  • LIPID ACCUMULATION in the intima becomes oxidized LDL and cholesterol clefts form - macrophages ingest this and become foam cells
50
Q

****What do you see here?

A
  • Cholesterol Clefts
  • Foam Cells
51
Q

What is the importance of cholesterol clefts in atherosclerosis?

A

• Cholesterol Clefts incite inflammation and Subsequent Release of IL-1

52
Q

****What cell type is shown on the vessel surface seen here?

A

• Foam Cells

53
Q

****What is this?

A

• Fibrous Cap of an atherosclerotic Plaque resembling granulation tissue

54
Q

What typically makes of the cells of a plaque and the ECM?

A

Cells:
• Smooth Muscle
• Macrophages
• T-cells

ECM:
• Collagen
• Elastic Fibers
• Proteoglycans
• Cholesterol Clefts

55
Q

****What is happening in this coronary artery?

A
  • Thrombosis seen as red
  • Recanalization of an old hemorrhage (seen as darker pink)
56
Q

*****Would you consider this a stable or unstable plaque? why?

A

Stable because only thickening of the wall is seen and no hemorrhage or thrombosis is evident

57
Q

*****Would you consider this plaque stable?

A

NO there is clear evidence of thrombus

58
Q

*****What is this?

A

*Thrombus formation in descending interventricular coronary artery

59
Q

****what process is seen here?

A

Thrombus from Ruptured Plaque

60
Q

What are some of the clinical complications of atherosclerosis?

A
  • Ischemia
  • MI
  • Stroke
  • Aortic Aneurysms
  • Peripheral Vascular Disease
61
Q

What layers are involved in aneurysms?

A

All Three Layers

62
Q

What is False Hematoma?

A

• Hematomas that communicate with the extravascular space

63
Q

What are the characteristic symptoms of an aneurysm?

A

• Deep constant pain in abdomen accompanied by back pain

64
Q

Why/How does atherlosclerosis put you at an increased risk of aneurysm?

A
  • While atherlosclerosis is a disease of the intima but the plaque may compress and cause thinning of the media
  • Weakening of the wall and loss of elasticity causes a predisposition for dilation and rupture
65
Q

*****What is this patient about to get surgery for?

A

Abdominal Aneurysm

66
Q

*****What disease causes a predisposition for the disease shown here?

A

Hypertension

• This is an ascending aortic dissection

67
Q

******what disease causes a predisposition for the disease seen here?

A

Atherlosclerosis

• this is an abdominal aortic aneurysm

68
Q

What genetic disorders put you at an increased risk of aneurysm?

A
  • Collagen Defects
  • Marfans or Type IV Ehlers-Danlos Syndrome
69
Q

Syphilis is most likely to cause what type of aneurysm? • why does this happen?

A

Thoracic
• Happens as a result of inflammation around the VASO VASORUM
• Inflammatory cells are often plasma cells

70
Q

****What pathological process is shown in this picture?

A

*Thoracic aneurysm

* Notice the Tree Bark Appearance

71
Q

*****What pathological process is shown here?

• Who is at the greatest risk of experiencing this?

A
  • Abdominal Aortic Aneurysm
  • Male Smokers over 50 years old
72
Q

Who is AAA typically seen in?

• complications?

A

Typically Male smokers over 50

Complications:

  • Obstruction of Vessels Branching off of the aorta
  • Embolism
  • Impingement on Adjacent Structures
  • Rupture
73
Q

How does AAA feel?

A

* Feels like a pulsating tumor in the abdomen

74
Q

****What processes is seen here?

A

• Dissection

75
Q

****What processes is seen here?
• main risk factor

A
  • Dissection of Ascending Aorta
  • Risk Factor - Hypertension
76
Q

What is the role of TGF-ß in the pathogenesis of Dissection?
• What is unique about aneurysms in people with TGF-ß dysregulation?

A
  • TGF-ß regulates smooth muscle cell proliferation and matrix synthesis
  • Mutations in TGF-ß receptors or Downsteam signaling pathways result in defective elastin and collagen synthesis
  • ANEURYSMS in these people tend to RUPTURE even when SMALL
77
Q

What is the pathophysiology that links Marfan Syndrome to Aneurysm?

A
  • FIBRILLIN is abnormally synthesized
  • TGF-ß is sequestered in aortic wall due to abnormal FIBRILLIN
  • this results in DYSREGULATED SIGNALING that causes progressive loss of elastic tissue
78
Q

Cystic Medial Degreneration

  • what is it?
  • what causes it?
A

What is it:
• Change in medial smooth muscle phenotype

Cause:

• ECM synthesis is defective due to ischemic changes of the outer media

79
Q

How can Dissection in a patient cause Cardiac Tamponade?

A

• Dissection can travel Retrograde into the heart valves

80
Q

****What is abnormal about the aortic wall shown here?

A

• Weak disorganized collagen can be seen which puts the patient at higher risk for Dissection or Aneurysm ***Disorganization at the top = major problem

Cardio - Gupta (12 decks)

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